The inflammatory process in MS is initiated by binding of pathogen-associated molecular patterns (PAMPs) from pathogens or commensal bacteria and damage-associated molecular patterns (DAMPs) from dead or dying cells to pathogen recognition receptors (PRRs), leading to activation of innate immune cells and production of IL-1, IL-6, IL-12, IL-18, and IL-23, cytokines that promote the differentiation and expansion of encephalitogenic Th1 and Th17 cells (101, 102). This evidence concerns the gene IL23A and myeloid sarcoma.